In 104 normal boys, aged 7 to 14 years (bone ages 5 to 15 years), plasma dehydroepiandrosterone (DHEA) rose from 52.7 at 7 years, to 112.0 ng/100 ml at 10 years. A further rise occurred at 12 years (188 ng/100 ml). In relation to the bone age, DHEA increased from a mean plasma level of 31.1 at a bone age of 5 years to 77.1 ng/100 ml at one of 7 years. Further increases were observed with mean values of 163.2 at a bone age of 11 years, and of 221.2 at a bone age of 12 years, with a maximum of 333.4 ng/100 ml at bone ages of 14-15 years. The first significant increase of plasma testosterone (T) was noted at a bone age of 12 years (54.8 ng/100 ml). The major rise of T was preceded by the rise of plasma LH and was accompanied by the rise of plasma FSH. Plasma DHEA and T were also measured in 123 normal girls, ages 6 to 13 years (bone ages 5 to 15 years). DHEA rose significantly from a mean level of 44.7 at 6 years, to 80.9 ng/100 ml at 8 years, with further increases between 9 and 10 years and between 10 and 11 years. In relation to bone age, DHEA increased significantly from a mean plasma concentration of 30.9 at a bone age of 5 years, to that of 58.6 ng/100 ml at 7 years. Further increases were observed with values of 191.1 at a bone age of 10 years and 485.6 ng/100 ml at a bone age of 13 years. The first significant rise of testosterone (T) occurred at 10 years of both chronological and bone age. DHEA rose before the increase of gonadotropins. The major rise of T at a bone age of 10 years occurred concurrently with increases in plasma FSH and LH. Low levels of DHEA were observed in Addison's disease. In hypogonadotropin hypogonadism and in anorchia, DHEA levels were normal, suggesting that DHEA is produced primarily in the adrenal gland. In seven girls with early adrenarche, plasma concentrations of DHEA were in the upper range of normal values, whereas T levels were within the normal range. Conversely in girls with late adrenarche, plasms DHEA was lower than normal but T was within the normal limits. The elevation of DHEA prior to the first signs of puberty suggests that DHEA may play a role in the maturation of the hypothalamic-hypophysealgonadal axis. However, the mechanism that triggers the secretion of DHEA is not known.

Pyridoxine-dependency is a rare autosomal recessive disorder causing a severe seizure disorder of prenatal or neonatal onset, psychomotor retardation and death in untreated patients. Treatment requires life-long supplementation with pyridoxine (vitamin B6). The underlying defect is unknown, and there is no biological marker for the disease. Clinical diagnosis is often delayed and severe neurological sequelae are common. This article summarizes both clinical and therapeutic aspects.

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Serum melatonin concentration in early morning during the menstrual cycle, studied in five healthy women, showed that melatonin was elevated at the time of menstrual bleeding and had its nadir at the time of the menstrual cycling in humans.

A radioimmunoassay for melatonin has been developed after the raising of anti-melatonin antibodies in rabbits. The radioimmunoassay is specific and the sensitivity range is greater than the tadpole bioassay.?Author

The plasma profiles of 8 hormones were followed over the course of prepuberty and puberty in 30 adolescent males who developed gynecomastia and 24 who did not. Throughout puberty, ratios of delta 4-androstenedione to estrone (E1) and estradiol (E2) were significantly lower in the gynecomastia group than in the control group. Similarly, ratios of dehydroepiandrosterone-sulfate to E1 and E2 were significantly lower in the gynecomastia group. In contrast, ratios of plasma testosterone to E1 and E2 as well as plasma progesterone and PRL concentrations, were similar in both groups. Because of the adrenal origin of dehydroepiandrosterone and its sulfate, and of peripheral conversion of adrenal androgens to E1 and to E2, it appears that either decreased adrenal production of androgens and/or increased conversion of dehydroepiandrosterone-sulfate and delta 4-androstenedione to estrogens cause transient gynecomastia in adolescent boys.

Tumour necrosis factor-alpha (TNF-alpha) is an important mediator in the pathogenesis of Gram-negative shock. In order to assess the role of TNF-alpha as a marker of the severity of infections in the neonates, serum TNF-alpha concentrations were determined at the time of septic work-up in 69 newborns (gestational age: 28-40 weeks). Nine patients had systemic infection (group A), four of them with signs of circulatory failure. Eleven patients had positive cultures of gastric aspiration or placental smears (group B) and 49 patients had completely negative septic work-up. Patients of group A had significantly more elevated serum TNF-alpha levels than patients of group B and C. Within group A, patients with circulatory failure had mean serum TNF-alpha concentration of 2165 +/- 817 pg/ml versus 27 +/- 8 pg/ml in newborns without shock. Serum TNF-alpha concentrations of more than 15 pg/ml detected systemic infections in eight out of nine patients. The specificity was 98% (1 elevated TNF-alpha concentration out of 60 non infected patients). These data indicate that premature neonates and term newborns are able to produce TNF-alpha when they are infected. Highly elevated TNF-alpha concentrations are found in severe systemic infections causing cardiovascular impairment.

Using a newly characterized anti-melatonin serum it has been possible to establish human serum melatonin concentrations at short time intervals during 24 h. A clear circadian rhythm with peak values during the dark phase was demonstrated in both men and women. Values (pg/ml; mean ± SE) were as follows: females 02.00 h: 130 ± 7, 18.00 h: 45 ± 5; males 02.00 h: 140 ± 11, 18.00 h: 70 ± 5. The estimation (pg/ml; mean ± SE) of melatonin in human serum (males: 63 ± 22 and females: 100 ± 45) and cerebrospinal fluid simultaneously taken has shown that melatonin is lower in cerebrospinal fluid (males: 59 ± 33 and females: 57 ± 28). Blanks are not subtracted.